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117 Cards in this Set
- Front
- Back
AE for magnesium IVP for torsades (what is going to happen if you give it fast)
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it's going to cause bradycardia- stop HR
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class Ia drugs-effect on heart (2) usage
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Decrease conduction velocity and increase action potential duration
Used most frequently for conversion of atrial flutter/fibrillation and maintenance of sinus rhythm |
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class Ib drugs- effect on heart (2)
usage (2) |
Minimal change in conduction velocity and slight decrease in action potential duration
Not useful for atrial arrhythmias Used for ventricular arrhythmias, especially those associated w/MI (but not for prophylaxis) |
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Class Ic drugs- effect on heart
usage |
Marked prolongation of conduction velocity- proarrhythmic
Used for atrial flutter/fibrillation in patients w/structurally normal hearts |
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Class Ia drugs- MoA - channel fx (2)
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block Na+ intermediate on/off rate-
and K+ channels |
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Class Ib drugs- channel fx
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Na+ fast on/off rate
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Class Ic drugs- channel fx
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Na+ slow on/off rate
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class II drugs
block what |
beta blockers
Ca+ channels...(indirect?) |
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Class III drugs- target
example |
K+ channel
amiodarone, sotalol, dofetilide |
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Class IV drugs
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non DHP CCBs
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Class III drugs- effect on heart
usage |
prolong action potential duration
used in both atrial and ventricular arr. |
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mnemonic for classes of antiarrhythmics
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N (sodium) O (I)
Boys (beta blockers) (II) Kiss (K+) (III) Carrie (Ca++) (IV) |
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Omissions from Vaughan Williams (2)
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adenosine
dig |
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adenosine pearls- what drugs will affect it (DDI) (2)
and hypersensitivity? |
Potentiated by dipyridamole (adenosine uptake inhibitor)
Inhibited by methylxanthines (block receptor)- if on gout shit have to give more adenosine Hypersensitivity in cardiac transplant (cut vagal nerve) patients can cause asystole |
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Type Ia drugs (3)
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Quinidine
Procainamide Disopyramide |
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3 characteristics of Ia drugs (moa)
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Moderate Na+ channel blocking
Decreased conduction velocity Prolonged repolarization |
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extra effects of quinidine (2)
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α-adrenergic block and vagolytic
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quinidine (other targets than Na+) (2)
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α-adrenergic block and vagolytic
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what happens if you give quinidine alone, or IV?
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HoTN (hypotension) when given IV
Acceleration in AV conduction if used alone (must combine w/ß-blocker) |
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quinidine metabolism (2 proteins)
implication? |
Hepatic metabolism- CYP2D6 and PgP (raises dig lvls- i guess more so with pgp)
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quinidine dosing IR and SR
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IR q6h- start with this, and convert to SR
SR q8-12h |
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7 AEs of quinidine
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N/V/Diarrhea 25-50%
Cinchonism- variety of AE (tinnitus, vertigo, blurred vision...) Bone marrow suppression Reversible thrombocytopenia Hemolytic anemia Hepatitis Lupus-like syndrome (drug fever) |
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Least anticholinergic of Ia class
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quinidine
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procainamide AE/tolerance (2)
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Better tolerated IV than quinidine
BUT 70% get anti-nuclear antibodies, especially slow acetylators resulting in Lupus-like syndrome (30% of long-term users) |
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you can go down from loading dose of procainamide early if...(3)
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QRS widens > 50%, significant HoTN, or arrhythmia abolished
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disopyramide usage (2)
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Rarely used except for hypertrophic cardiomyopathy and neurocardiogenic syncope
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disopyramide effect on heart
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very negative inotropic effect
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Class I antiarrhythmics- avoid in what condition
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HF!!!
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disopyramide AE (why it isn't used) (3)
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Prominent anticholinergic effects (dry mouth, urinary retention, constipation, blurred vision)
N/V Hepatic cholestasis |
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disopyramide metabolism
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CYP3A4
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Type Ib drugs (2)
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Lidocaine
Mexiletine |
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characteristics of Ib drugs (3)
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Mild Na+ channel blocking
Shortened repolarization Slight decrease in conduction velocity |
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lidocaine route- why?
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Given IV d/t hepatic first-pass metabolism
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dosing of lidocaine- adjustments? (2)
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decreases dose in liver and heart failure
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lidocaine- metabolism effects/monitoring
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inhibits it's own metabolism- so in hospital you have to get daily level of the drug (level will increase)
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AE for lidocaine (3)
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Neurologic (paresthesias around mouth, sedation d/t accumulation of MGX metabolite in renal failure, tremor, nystagmus, delirium, seizures)
Less GI toxicity relative to mexiletine AV block |
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lidocaine metabolism enzymes (2)
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CYP3A4 and 2D6 substrate
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mexilitene- what is it
metabolism route |
PO equivalent to lidocaine
Hepatic metabolism |
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mexiletine AE (2)
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GI (take w/food), occasionally CNS
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other...besides lidocaine...infrequently used Ib drugs (2)
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Phenytoin
tocainide |
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tocainide AE (2)
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bone marrow suppression, pulmonary fibrosis
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Ic drugs (2)
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Flecainide
Propafenone |
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Ic drug properties (3)
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Significant Na+ channel blocking
Decreased conduction velocity No effect on repolarization |
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Flecainide- what is it
usage (3) |
Minor K+-channel blocker
Occasionally used in AVNRT (nodal re-entrant tachy) or Afib mostly used for vt |
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flecainide mortality rates- when/why
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Increased mortality after MI in CAST (can cause monomorphic VT)
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3 categories for AE in flecainide
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cardiac
CNS GI |
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flecainide metabolic enzyme
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CYP2D6 substrate
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cardiac AE for flecainide (3)
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Cardiac: AV block, HF, proarrhythmic
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CNS AE for flecainide (3)
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CNS: dizziness, headache, blurry vision
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GI/mouth AE for flecainide (2)
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GI: dysgeusia (metallic taste), N/V
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propafenone- additional activity
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S-enantiomer is ß-blocker
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propafenone- metabolism (3)
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Substrate of CYP2D6, 3A4, and 1A2
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selective metabolite of propafenone and what it targets
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5-OH propafenone blocks Na+ channels but not ß receptors
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propfenone DDIs (3)
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Increases digoxin (~ 80%), warfarin, metoprolol
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propafenone- renal/hepatic disease dosing
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Renal and hepatic dose adjustments...
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propafenone cardiac AE (30
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Cardiac: QTc prolongation, AV block, HF
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propafenone GI AE (3)
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metallic taste, dry mouth, constipation
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moricizine (2) what is it
use? |
Phenothiazine derivative
Increased mortality after MI in CAST-II so not used |
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only class of drugs that reduce mortality in arr.
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class II (BBs)
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beta blockers (class II) effect on heart (4)
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Lowers sinus conduction rate
-Decreased conduction velocity -Increased refractory period Prolong action potential and slow heart rate |
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6 AE for BBs
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HF
Depression Bronchospasm Impotence Fatigue AV block |
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Class III drugs (4)
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Amiodarone
Dofetilide Ibutilide Sotalol (d-isomer) |
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Type III drug effects on heart (2)
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Significant K+ channel blocking
Prolongation of refractory period |
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amiodarone- drug properties
MoA (principal) |
Broad spectrum class III agent w/effects in all 4 Vaughn-Williams classes
Principal MOA = delaying repolarization |
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amiodarone usage (2)
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Safe in both atrial and ventricular arrhythmias
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amiodarone- 8 categories of AE
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cardiac
pulmonary thyroid ocular neuro derm hepatic GI |
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amiodarone cardiac AEs (2)
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HF (usually well tolerated in these patients)- because of BB property- but still the only drug other than dofentilinide that can be used in HF
Torsades (< 1% due to QT prolongation, but less than other class III agents) |
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pulmonary AE for amiodarone
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3% of patients may get pulmonary fibrosis or delayed hypersensitivity pneumonitis
ergo Patient MUST report unexplained dyspnea, cough, or fever |
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half life of amiodarone
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58 days...
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thyroid AE of amiodarone (2) why?
do you treat? |
44% of drug is iodine
Hypo- or hyperthyroidism do not give treatment of subclinical hypothyroidism! |
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ocular AE for amiodarone- main one
when this becomes and issue monitoring |
Corneal deposits occur in nearly all patients so treatment needed
only issue if they get Halos, photophobia, and overt retinopathy may occur Eye exam (w/slit lamp) yearly |
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neuro AE of amiodarone (3)
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Tremor, ataxia, peripheral neuropathy in 20-40% of patients (tremor not uncommon w/long-term therapy)
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derm AE of amiodarone (2)
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sun exposed skin = blue tinge (smurfing)
Photosensitivity! use sunscreen |
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hepatic AE of amiodarone (2)
hepatitis? monitoring |
Asymptomatic transaminitis and hyperbilirubinemia in 4-25%
Rarely hepatitis so just monitor LFTs q6months |
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GI AE of amiodarone (3)
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N/V (mostly with loading doses)
Loss of taste Constipation |
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DDIs of amiodarone (major ones)
(5 drugs) HUNDREDS of DDIs |
digoxin
warfarin Increases levels of BBs, phenytoin, theophylline |
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dig/warfarin + amiodarone- how to handle (2)
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dig- empirically reduce dose by 50%
warfarin- reduce dose by 30% |
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8 monitoring things for amiodarone fuck
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CXR, EKG q3-6months (fibrosis)
Thyroid (S/sx hypothyroidism), LFTs q6months Annual eye exam Continuous dry cough ± dyspnea Nausea should diminish with time Photosensitivity |
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dronederone- SAR (3)
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amiodarone relative
removed iodines to lower thyroid issues methylsulfonamide group to reduce lipophilicity and reduce neurotoxic fx BA sucks |
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dronedarone fx on SCr
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elevates SCr but doesn't affect renal fxn
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dronedarone half life
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16 h much much shorter than amiodarone
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dronedarone HUGE CI ****
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dronederone- big issue- CONTRAINDICATED IN HF ( i guess decompensated was the one that was studied)
so...just...use amiodarone |
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dronederone- metabolism/DDIs
interacts with what 2 proteins which drugs? (2) what drug does it not interact with, that amiodarone does? |
Metabolized by CYP3A4/competes for PgP
drug interactions: ketoconazole increases AUC 15 fold Digoxin increases by 2.5x- due to pgp competition No warfarin interaction (amiodarone does) |
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in pt with persistent AF- amiodarone vs. dronederone
results |
cardioversion -->then dronederone or amiodarone
AF recurrence was higher in dronedarone but fewer ADRs with drone- less effective less adherence with amiodarone |
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Contraindications for dronederone (2)
not studied in what pop |
HF (IV, and II-III if decompensated, within last month)
Qt prolongation not studied in hepatic/pregnancy Not studied in hepatic or pregnant women |
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AE for dronederone (4)
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GI/bradycardia/QT prolongation/SCr increase
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indications for dofetilide
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Conversion and maintenance of AF (only atrial arr.) to NSR
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AE of dofetilide (4)
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Cardiac: 3-6% risk of Torsades
CNS: headache, dizziness Chest pain |
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2 DDIs with dofetilide (out of a million)
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hctz, bactrim
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2 antiarr. safe to use in HF
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dofetilide
amiodarone |
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dofetilide CI (1 CI, 1 other)
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Contraindicated if QTc > 500 msec
must be hospitalized for 3 days |
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dofetilide metabolism
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CYP3A4 substrate
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risk for torsades with dofetilide increases with...(3)
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Risk increases w/renal insufficiency, prolonged baseline QTc, other QTc prolonging drugs (fluconazole, haloperidol, fluoroquinolone)
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ibutilide- main AE
when will this AE occur? (2) |
2-5% incidence of Torsades
most likely will occur within first 24 h or pt with HF |
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ibutilide DDI
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none
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ibutilide monitoring
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Continuous EKG monitoring for first 4 hours of infusion
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sotalol- properties (4)
what is it potency as a BB 2 others |
BB w/class III properties
Not that potent of BB Minimal effect on PR intervals- idk why Proarrhythmic |
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sotalol- which eniantomer is antiarrhythmic?
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Only d-sotalol is antiarrhythmic
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sotalol- "place" and therapy
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Typically second-line after amiodarone- better for younger pt (due to AE of amiodarone)
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8 sotalol ADRs
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Dose-dependent increase in QTc interval (and torsades)
AV block HoTN HF Bronchospasm Depression Fatigue Impotence |
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when would you d/c sotalol due to QTc interval prolongation
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>520
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sotalol + other BB for rate control? is this ok?
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yes- for rate control it's ok because sotalol is so weak
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5 characteristics/effects on heart of type IV antiarrhythmics
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Calcium channel blocking
Decreased sinus rate Slow conduction Prolong refractoriness Decrease automaticity |
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Type IV (CCB)- usefulness/indication (2)
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Useful for controlling ventricular response in AF
exercise-related tachycardias |
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verapamil/diltiazem ADR (5)
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GI: constipation**worse in verapamil, anorexia, nausea
Peripheral edema Hypotension |
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verapamil enzymes/proteins it interacts with (3)
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CYP3A4 and 1A2 substrate
CYP3A4 inhibitor P-glycoprotein inhibitor |
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CCBs in CHF
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neg inotropic effect limits use in HF- though diltiazem has less (can see it sometimes if stable HF)
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diltiazem DDIs (2)
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CYP3A4 substrate and inhibitor
P-glycoprotein inhibitor |
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digoxin uses (2)
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Atrial fibrillation with RVR (negative chronotrope)
Heart failure for morbidity benefit only (positive inotrope) |
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digoxin- dosing- use what weight?
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Does not distribute into adipose tissue → IBW
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half life of digoxin
elimination route? |
Half-life at steady-state = 36 h (24-46 h)
mostly renal: only 15% of digoxin is eliminated non-renally |
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therapeutic range for HF vs AF for digoxin
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1-2 mcg/mL for AF
0.5-1 mcg/mL for HF |
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3 major DDIs with dig
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quinidine
amiodarone verapamil |
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verapamil + dig- how to alter dig dose
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Decrease dose by 25% if concomitant verapamil
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quinidine/amiodarone + dig- how to alter dig dose
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Halve dose if concomitant quinidine and amiodarone
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disease state interactions and what to do with dose- digoxin (4)
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Reduce dose for untreated hypothyroidism
increase dose if untreated hyperthyroidism Reduce in renal failure Reduce in HF |
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digoxin toxicity sx (5)
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Fatigue
confusion/agitation/hallucinations GI: N/V/D Visual symptoms (halos) CV- anything you can think of (think of van gogh) |